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10.1038/mi.2014.129 http://scihub22266oqcxt.onion/10.1038/mi.2014.129 C4430298!4430298!25603826     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Mucosal+Immunol 2015 ; 8 (5): 1021-30 Nephropedia Template TP {{tp|p=25603826|t=2015. The Axl receptor tyrosine kinase is a discriminator of macrophage function in the inflamed lung |pdf=|usr=}}{{25603826}} gab.com Text The Axl receptor tyrosine kinase is a discriminator of macrophage function in the inflamed lung JO: Mucosal Immunol http://www.kidney.de/pget.php?&tw=1&pmid=25603826 #FOAvip Much of the biology surrounding macrophage functional specificity has arisen through examining inflammation-induced polarizing signals, but this also occurs in homeostasis, requiring tissue-specific environmental triggers that influence macrophage phenotype and function. The TAM receptor family of receptor tyrosine kinases (Tyro3, Axl and MerTK) mediates the non-inflammatory removal of apoptotic cells by phagocytes through the bridging phosphatidylserine-binding molecules growth arrest-specific 6 (Gas6) or Protein S. We show that one such TAM receptor (Axl) is exclusively expressed on mouse airway macrophages, but not interstitial macrophages and other lung leukocytes, under homeostatic conditions and is constitutively ligated to Gas6. Axl expression is potently induced by granulocyte-macrophage colony-stimulating factor expressed in the healthy and inflamed airway, and by type I interferon or Toll-like receptor-3 stimulation on human and mouse macrophages, indicating potential involvement of Axl in apoptotic cell removal under inflammatory conditions. Indeed, an absence of Axl does not cause sterile inflammation in health, but leads to exaggerated lung inflammatory disease upon influenza infection. These data imply that Axl allows specific identification of airway macrophages, and that its expression is critical for macrophage functional compartmentalization in the airspaces or lung interstitium. We propose that this may be a critical feature to prevent excessive inflammation because of secondary necrosis of apoptotic cells that have not been cleared by efferocytosis.Supplementary information: The online version of this article (doi:10.1038/mi.2014.129) contains supplementary material, which is available to authorized users. Twit Text FOAVip The Axl receptor tyrosine kinase is a discriminator of macrophage function in the inflamed lung ????Mucosal Immunol http://www.kidney.de/pget.php?&tw=1&pmid=25603826 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25603826 #FOAvip English Wikipedia <ref>{{Cite pmid|25603826}}</ref> The Axl receptor tyrosine kinase is a discriminator of macrophage function in the inflamed lung #MMPMID25603826 Fujimori T; Grabiec AM; Kaur M; Bell TJ; Fujino N; Cook PC; Svedberg FR; MacDonald AS; Maciewicz RA; Singh D; Hussell T Mucosal Immunol 2015[]; 8 (5): 1021-30 PMID25603826show ga Much of the biology surrounding macrophage functional specificity has arisen through examining inflammation-induced polarizing signals, but this also occurs in homeostasis, requiring tissue-specific environmental triggers that influence macrophage phenotype and function. The TAM receptor family of receptor tyrosine kinases (Tyro3, Axl and MerTK) mediates the non-inflammatory removal of apoptotic cells by phagocytes through the bridging phosphatidylserine-binding molecules growth arrest-specific 6 (Gas6) or Protein S. We show that one such TAM receptor (Axl) is exclusively expressed on mouse airway macrophages, but not interstitial macrophages and other lung leukocytes, under homeostatic conditions and is constitutively ligated to Gas6. Axl expression is potently induced by granulocyte-macrophage colony-stimulating factor expressed in the healthy and inflamed airway, and by type I interferon or Toll-like receptor-3 stimulation on human and mouse macrophages, indicating potential involvement of Axl in apoptotic cell removal under inflammatory conditions. Indeed, an absence of Axl does not cause sterile inflammation in health, but leads to exaggerated lung inflammatory disease upon influenza infection. These data imply that Axl allows specific identification of airway macrophages, and that its expression is critical for macrophage functional compartmentalization in the airspaces or lung interstitium. We propose that this may be a critical feature to prevent excessive inflammation because of secondary necrosis of apoptotic cells that have not been cleared by efferocytosis.Supplementary information: The online version of this article (doi:10.1038/mi.2014.129) contains supplementary material, which is available to authorized users. äThe Axl receptor tyrosine kinase is a discriminator of macrophage func(epmc).pdf DeepDyve Pubget Overpricing